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. 2018 Jan;20(1):30-37.
doi: 10.1177/1098612X17699723. Epub 2017 Mar 28.

Immunohistochemical evaluation of the activation of hepatic progenitor cells and their niche in feline lymphocytic cholangitis

Corma Ma Otte  1 , Chiara Valtolina  1 , Sandra Vreman  2 , Siobhan Hubers  1 , Monique E van Wolferen  1 , Robert P Favier  1 , Jan Rothuizen  1 , Louis C Penning  1
Affiliations

Immunohistochemical evaluation of the activation of hepatic progenitor cells and their niche in feline lymphocytic cholangitis

Corma Ma Otte et al. J Feline Med Surg. 2018 Jan.

Abstract

Objectives The aim of the study was to compare the hepatic progenitor cell niche in healthy feline livers and the liver tissue of cats with lymphocytic cholangitis. Methods Immunohistochemical stainings for vimentin, laminin, beta (β)-catenin and Notch1 intracellular domain (NICD) were used on formalin-fixed liver biopsies from affected (n = 12) and unaffected cats (n = 2). Results All immunohistochemical markers used were expressed in more cells, or more intensely, in the liver tissue of cats with lymphocytic cholangitis than in the liver tissue of unaffected cats. Conclusions and relevance Enhanced expression of vimentin, laminin, cytoplasmic/nuclear β-catenin and NICD in liver biopsies from cats with lymphocytic cholangitis indicates that the hepatic progenitor cell (HPC) niche is remodelled and activated. HPCs might provide insights into new regenerative treatment options for lymphocytic cholangitis in cats in the future.

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Conflict of interest statement

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Figures

Figure 1
Figure 1
Immunolocalisation of the expression of hepatic progenitor cell markers in (a,d,g,j) unaffected and (b,c,e,f,h,i,k,l) liver tissue from cats with lymphocytic cholangitis (LC). (a) Weak vimentin expression in the extracellular matrix (ECM) and vascular smooth muscle of unaffected liver (C2), and (b [LC4]) and (c [LC5]) strong vimentin expression in portal structures in diseased liver. (d) Weak laminin expression in the ECM of (C2) unaffected liver and (e [LC6]) moderate to (f [LC2]) strong expression of laminin in the ductular reaction in diseased liver. (g) Moderate-to-strong expression of β-catenin in the membranes of hepatocytes and cholangiocytes in (C1) unaffected liver and (h [LC3]) and (i [LC6]) moderate-to-strong expression of β-catenin in membranes and cytoplasm/nucleus of hepatocytes and ductular structures in diseased liver. (j) Weak Notch1/Notch1 intracellular domain expression in (C1) unaffected liver and (k [LC5]) and (l [LC1]) weak-to-strong expression in the portal structures in diseased liver
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